Serum concentrations of 25‐hydroxyvitamin D (25‐OHD), 24, 25‐dihydroxyvitamin D [24, 25‐(OH)2D], and 1α, 25‐dihydroxyvitamin D [1, 25‐(OH)2D] were measured in 30 ambulatory adult epileptic patients during long‐term anticovulsant treatment with phenytoin, phenobarbital, or carbamazepine. For the entire group, serum 24, 25‐(OH)2D was decreased (p < 0.0005) as compared to normal subjects to a mean value of 0.7 ± 0.1 (SEM) ng/ml. However, serum 1, 25‐(OH)2D was increased at 50 ± 7 pg/ml (p < 0.025). Serum 25‐OHD declined insignificantly to 19 ± 3 ng/ml. All three drugs caused a significant reduction of serum 24, 25‐(OH)2D concentrations. A significant decrease in serum 25‐OHD was observed only for the phenobarbital‐treated patients. Serum 1, 25‐(OH)2D was high in patients receiving phenytoin or carbamazepine but not in those taking phenobarbital. The finding suggest that while various anticonvulsant drugs appear to exert different effects on vitamin D metabolism, a universal finding is diminished serum 24, 25‐(OH)2D. The results support the notion that 24, 25‐(OH)2D deficiency may play an important role in the pathogenesis of anticonvulsant‐induced osteomalacia.
ASJC Scopus subject areas
- Clinical Neurology